FARMAKOLOGI BEBAN STUDI = 3 SKS Kuliah = 2 SKS dan Praktikum = 1 SKS

Presentasi berjudul: "FARMAKOLOGI BEBAN STUDI = 3 SKS Kuliah = 2 SKS dan Praktikum = 1 SKS"— Transcript presentasi:

1 FARMAKOLOGI BEBAN STUDI = 3 SKS Kuliah = 2 SKS dan Praktikum = 1 SKS Dosen Pengasuh : 5 Orang GBPP SAP yang telah disepakati terdiri dari : 1. Farmakologi Umum (4 jam) 2. Obat ANS & Relaksasi otot (6 jam) 3. Obat Anestesi lokal & umum (4 jam) 4. Obat Diuretik (2 jam) 5. Obat Sedatif-Hipnotik & CNS Stimulan (2 jam) 6. Obat Analgesik, antipiretik & antiinflamasi (2 jam) 7. Obat Hemostatika (2 jam) 8. Hormon & Uterotonika (2 jam) 9. Histamin dan Antihistamin (2 jam)

2 Pembobotan Penilaian Mata Kuliah :
1. Tugas : bobot 1,5 = 13,64% 2. Kuis/tentamen dll : bobot 1,5 = 13,64% 3. Soft skill : bobot 1 = 9,09% 4. UTS : bobot 2 = 18,8% 5. UAS : bobot 3 = 27,27% 6. Praktikum : bobot 2 = 18.18% bobot 11 = 100% Presensi : Wajib kuliah : Nilai E minimal 75% Nilai D,C & BC minimal 50%

3 PRAKTIKUM (1 SKS) GBPP  SAP disepakati 6 materi praktikum :
1. Cara pemberian obat 2. Obat yg berpengaruh thd. Tekanan darah 3. Mengenal stadium anestesi umum 4. Obat yg berpengaruh pada Diuresis 5. Obat menurunkan rasa nyeri 6. Obat penghambat inflamasi. Presensi : Wajib Praktikum 100% Kelompok Praktikum  Dibagi 6 kelompok : A1 dari kelas A nomor urut 1-45 A2 dari kelas A nomor urut 46-69 B1 dari kelas B nomor urut 1-55 B2 dari kelas B nomor urut 56-70 C dari kelas C ; dan D dari kelas D

4 GENERAL PHARMACOLOGY BY : D.K. Meles

5 PHARMACOLOGY PHARMACON = Drug/ Poison LOGOS = Science
PHARMACOLOGY : Science to Study of drug DRUG : All of substance to influence life system  application to prevent, diagnostic and therapeutics SCOPE OF PHARMACOLOGY - PHARMACOKINETIC PHARMACODYNAMIC PHARMACOTHERAPEUTIC PHARMACOGNOSI TOXICOLOGY

6 DRUG  All of Substance to influence life process in use to prevent, therapeutics and diagnostic of disease. Have criterion : 1. Effectiveness & Rivesible effect 2. Savety (Margin of savety)  Therapeutics Index. 3. High Selectivity

7 PHARMACOKINETIC ABSORPTION DISTRIBUTION BIOTRANSFORMATION EXCRETION

8 ABSORPSI OBAT : Moving Process or to remove of drug from tissue to another tissue  to cross the membrane with spesific mechanism. TRANSPORT PASIVE Different Concentration, No need Energy, non spesific DIFFUSION NON-IONIC FILTRATION  POROUS FASCILITATIVE DIFFUSION  CARRIER TRANSPORT ACTIVE OPPOSITION GRADIENS CONCENTRATION, Need Energy & Spesificity 3. PINOSITOSIS/ EXOSITOSIS/ ENDOSITOSIS.

9 DRUG ABSORBTION  Account in % from drug dose
DRUG BIOAVAILABILITY Prosentage drug to reach site of action. Was count from dose of drug (for drug sistemik only). FACTOR2 TO INFLUENCE RATE OF DRUG ABSORBTION : 1. Route of drug application 2. Circulation of place application drug. 3. Solubelity of drug 4. Ionization Rate of Drug 5. Broad of absorbtion area. 6. Size of molecule particle of drug 7. Drug Formulation

10 ROUTE OF DRUG ADMINISTRATION
1. ENTERAL (SUBLINGUAL, PER-ORAL, PER-ANAL) 2. PARENTERAL (SC., IM., IV., INTRAPERITONEAL) 3. TOPICAL (SKIN, MUCOSA) 4. PERINHALATION. Sub-Lingual : Condition :  Iritation, Damage by gastric Acid &Damage from drug metabolis.To clause  Dilute in saliva, Non-iritan & Lipofilik.

11 PER-ORAL : Rate of absorbtion irreguler, Sometimes rectum irritation
General, easy, safety and cheap. Influenced by GIT motility Absorbtion  Diffusi pasive, depend on rate of disolution & disintegration. No application in consciousless. PER-RECTUM Applicated in condition : gastric iritation, vomiting, damage by gastric acid. Rate of absorbtion irreguler, Sometimes rectum irritation

12 Per-injection : Benefid : Quick in absorbtion, vomit condition consciousless and emergency applicated Wickedness : must be sterilzation, can”t self uses, pain, & ralative more expensive. Intra-Vena : No absorbtion process  direct in blood Onset dan Duration  quickly Iritatif drug can applicated Drug toxicity  Low in therapeutics Index Must be carefully

13 Intra-muskuler (I.M.) dan Sub-kutan (S.C.)
Condition : non-iritan drug, water soluble or suspention form. Quick in effect (im=Sc). Intraperitoneal : In animal experimental applicated only opten infection. Subtitute i.v. route Per-inhalation : Use in gas form drug. Absorbtion a cross epithel mucosa & quick. Need tools/ specific methode Dificult in dose count Topical  Unguentum, drops for mocosa & skin

14 DRUG DISTRBUTION AFTER ABSORBTION 
Extracelluler Fluids (Plasma + 4%,Interstesiil + 13%). DRUG  Protein plasma bound, Inactivation/ metabolism process,  Bound in reseptor Respon/ drug effect,  Exretion  Renal Intraseluler Fluid + 41% DRUG  Reseptor  drug respons  Prot. tissue.  Non Spesific & Reversibel.  Bound in Fat  Drug Reservoir.  Metabolism (Biotransformation). Drugs lipid soluble easy a cross membrane and distribution to intracelluler fluids, distribusi ke intraseluler. Opposite on non lipid soluble drug

15 BIOTRANSFORMATION: * Decrease in fat solublelity * to break in ionized
MECHANISME TO CHANGE DRUGS STRUCTURE TO BE : * Decrease in fat solublelity * to break in ionized * Decrease in protein plasm/ tissue bound. Biotransformation  Drug to be in active Metabolite Aktive : Prontosil (In vitro)  Sulfanilamid. Proguanil  Metabilite aktif.

16 MECHANISME OF BIOTRANSFORMATION
DRUG ABSORBTION DISTRIBUSTION protein bound reseptor bound Excretion BIOTRANSFORMATION (metabolism) FASE I FASE II Oksidation cytochrom axidase Sulfation Sulfonyl transferase Reduction Declorinasi Glucorhonidation G.transferase 3. HidrolysisEsterase, Amidase Conjugation As.Glukoronat 4. Hydrasi Hidrolase AcetYlation, Methylation BM < BM> BM< 300 URINE Filtration, Secretion

17 PHARMAKODYNAMIC Pupose : To know drug effect To know drug Interaction
To know spectrum drug respons MECHANISM OF ACTION : Interaction with drug reseptor  to change biochemical & Physiological process ( Neurotransmitter) Respons. Physical-chemist Characteristic of drug  Drug respons Chelating Agent  drug respons Drug incorporation with celluler structure  drug respon

18 DRUGS INTERACTION SYNERGISM  ADITIVE & POTENTIATIVE ANTAGONISM :
* A. Chemist : Heparin X Protamin * A. Functional/Physiological ( NE X Histamin) * A. Selective  Receptor – Drugs. A. Selective Competitive : In seem receptor. Riversible : ACH x Atropin Irreversible : NE x Prazosin A. Selective non-competitive  Different receptor, D-R bound can”t break in highly dose. Papaverin x Histamin ( Papaverin x ACH)

19 DOSE : measure / quantity of drug to give for individual until a cross activity threshold but can”t cross Toxicity threshold. Margin Of safety = LD50 : ED50 INFLUANCE FACTOR OF DOSE : BODY WEIGHT( BW) OLD RUST SeX Time of administration Patological Disholder Genetic factor Tolerance

20 DRUG TOXICITY Wrong in drug administration : Tetracycline (I.V)  konvulsive. Penicilline (I.V.)  Presipitation. To remain the drug effect ( Excessive dose/ Over dose, Ren & liver malfunction, genetic factor, drug interaction). Hypersensitive reaction (Allergy) : Dermatitis, Asthma, Shyok anafilactic, damage in liver & ren, damage in bonemarrow. Blood discrasia, as well as Leucopenia, aplastic anaemia, haemolytic anaemia, thrombositopenia. Toxicity in liver & ren Teratogenic effect.

21 RESEARCH OF DRUG TO INVENTION THE NEW DRUG  * EMPERICALLY
* RASIONALITY * UNEXPECTED (KEBETULAN) * SCREENING PROCESS 2. PREKLINIK TRIAL  * Activity Test & Side effect Test * Uji Pharmacokinetic dan Pharmacodynamic * Uji Farmacy yang meliputi : * Uji Kualitative dan Kuantitative bahan * Uji Stability * Uji Sifat Physic dan Chemist * Uji drug formulation * Uji general toxicity : Uji Acute , Sub Acute & Chronic Toxicity Test * Uji specific toxicity : Uji Teratogenic, Mutagenic dan Carcinogenic 3. KLINICAL TRIAL  Devide 4 fase dan Uji Monitoring drug side effect (MESO).

22 SEMOGA BERMANFAAT